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CXCR4 expression on monocytes is up‐regulated by dexamethasone and is modulated by autologous CD3 + T cells
Author(s) -
Caulfield Jason,
Fernandez Maria,
Snetkov Vladimir,
Lee Tak,
Hawrylowicz Catherine
Publication year - 2002
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.0019-2805.2001.01359.x
Subject(s) - monocyte , peripheral blood mononuclear cell , cd3 , chemokine , stromal cell , cxc chemokine receptors , chemokine receptor , biology , receptor , microbiology and biotechnology , inflammation , immunology , antigen , cancer research , in vitro , biochemistry , cd8
Summary Chemokines and their receptors regulate cell migration to sites of inflammation. The glucocorticoid dexamethasone has potent anti‐inflammatory effects, yet paradoxically up‐regulates expression of some cytokine receptors. We have examined the effects of dexamethasone on chemokine receptor expression. Using an RNase protection assay, we show that dexamethasone up‐regulates human peripheral blood mononuclear cell (PBMC) expression of CXCR4 mRNA. Flow cytometric analysis demonstrated that increased expression of CXCR4, but not CXCR1 and CXCR2, occurred on both monocytes and CD3 + T cells in PBMC mixed cultures. A stromal‐derived factor (SDF)‐1α‐mediated calcium influx was detected on monocytes. Basal levels of CXCR4 expression on purified monocytes were lower when compared with monocytes in mixed PBMC cultures. Co‐culture of monocytes with purified CD3 + T cells led to enhanced basal expression of CXCR4 on monocytes. The use of transwells to partition CD3 + T cells resulted in increased CXCR4 expression on monocytes, suggesting that CD3 + T‐cell derived soluble factors regulate CXCR4 expression.